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. 2022 May 6;15:847440. doi: 10.3389/fnmol.2022.847440

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Copyright © 2022 Wang, Ren, Wu, Liu, Wei, Ding, Zhou, Xu and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Diagram of NLRP3 inflammasome-related mechanisms after cerebral I/R injury. The involvement of NLRP3 inflammasome in the pathogenesis of cerebral I/R injury mainly includes two aspects: inflammation and pyroptosis. NLRP3 inflammasome is expressed in microglia, neuron, and endothelial cell to regulate inflammation after cerebral I/R injury. In addition, NLRP3 inflammasome is expressed in astrocytes, oligodendrocytes, microglia, neuron and endothelial cell involved with pyroptosis in ischemic tissue. In this figure, we also conclude the pathways in this review, which regulate the activation and inhibition of NLRP3 inflammasome in cerebral I/R injury. The upward arrow represents the suppression of NLRP3 inflammasome, and the downward arrow represents the activation of NLRP3 inflammasome. NLRP3, pyrin domain-containing protein 3; I/R, ischemia–reperfusion.